The CD38 Knockout 143B Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout population of human 143B osteosarcoma cells with targeted disruption of the CD38 gene. This polyclonal pool, generated without single-cell cloning, offers a genetically diverse loss-of-function model suitable for investigating CD38 biology in a bone cancer context. The cells are expanded from a mixed population of edited clones, ensuring a broad representation of mutations and facilitating robust, population-level analyses.
The host 143B cell line is a highly metastatic, HOS-derived human osteosarcoma model extensively used to study tumor progression and metastasis. These cells retain aggressive growth characteristics, high tumorigenicity, and pulmonary metastatic potential in vivo, making them an ideal platform for knockout studies. The 143B line endogenously expresses key signaling factors such as PI3K, AKT, mTOR, and NF-??B, which are often dysregulated in osteosarcoma and intersect with CD38-regulated pathways.
CD38 encodes a multifunctional ectoenzyme and receptor that catalyzes the conversion of NAD+ into cADPR and NAADP, second messengers that mobilize intracellular calcium. CD38 expression is induced by TNF-alpha, IL-1beta, interferon-gamma, all-trans retinoic acid, and vitamin D3. Downstream, CD38-generated calcium signals activate ryanodine receptors, CaMKII, calcineurin, NFAT, and MAPK/ERK, while also augmenting PI3K/AKT and NF-??B cascades. Additionally, CD38 interacts with CD31/PECAM-1, hyaluronan, caveolin-1, and CD11b/CD18, influencing cell adhesion and immune recognition.
In the 143B osteosarcoma context, CD38 knockout cells enable dissection of CD38??s role in calcium-mediated proliferation, migration, and apoptosis, as well as in NAD+ metabolism. Osteosarcoma often features aberrant PI3K/AKT and NF-??B activation, and loss of CD38 is expected to perturb these pathways, providing a model to test CD38-targeted therapies such as daratumumab. This knockout also aids in studying CD38-dependent microenvironmental interactions via CD31 binding, which may impact metastatic behavior.
Typical applications include calcium mobilization assays (Fluo-4), cADPR and NAD+ quantification, MTT proliferation assays, Transwell migration/invasion studies, and drug sensitivity profiling. The polyclonal nature supports pooled CRISPR screens, RNA-seq, and phospho-signaling analyses (p-AKT, p-ERK, p-NF-??B). Researchers can employ co-immunoprecipitation to probe CD31/CD38 interactions or examine senescence and immunometabolism. For further technical information, custom requests, or support, please contact Ascent Research.
